BRS4 → BRS1 — Bioenergetic Support for Neurotransmission
Mitochondrial ATP supply and related energetic signalling constrain synaptic and neurotransmitter work in BRS1.
Dependency
BRS4 maintains neuronal energy availability through mitochondrial ATP generation and activity-coupled bioenergetic signalling. Synaptic transmission is energetically expensive; insufficient ATP supply can limit the conditions under which BRS1 sustains signalling.
Principal Routes
| Route | Contribution to BRS1 | Relationship |
|---|---|---|
| Mitochondrial ATP supply for synaptic signalling | Enables the energy cost of neurotransmission | Direct |
| Mitochondrial signalling and redox coupling | Shapes the intracellular environment of synapses | Conditional |
Network Interpretation
This is a resource constraint rather than a transmitter-synthesis pathway. BRS4 does not specify which neurotransmitter is released; it sets whether signalling can be energetically sustained. Chronic stress and glucose dysregulation may reach BRS4 through BRS6 (BRS6 → BRS4), so some BRS1 energetic strain is mediated rather than native to BRS4 alone.
Boundary and Evidence Status
Synaptic energy dependence is established neurophysiology. Treating BRS4 as an upstream constraint on BRS1 is a framework interpretation. The relationship does not establish that raising mitochondrial nutrients improves neurotransmitter function or ADHD outcomes.
Supporting Evidence
- Harris et al., 2012 — Reviews synaptic energy use and supply, showing that signalling accounts for a large share of neuronal ATP demand.
- Picard, 2015 — Reviews mitochondria as signalling and energetic organelles coordinating cellular energetics with neuronal activity.